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南蛇藤籽油和有机提取物减轻过氧化氢和谷氨酸诱导的胚胎大鼠前脑神经元细胞损伤。

Celastrus paniculatus seed oil and organic extracts attenuate hydrogen peroxide- and glutamate-induced injury in embryonic rat forebrain neuronal cells.

作者信息

Godkar P B, Gordon R K, Ravindran A, Doctor B P

机构信息

Department of Biochemical Pharmacology, Division of Biochemistry, Walter Reed Army Institute of Research, 503 Robert Grant Avenue, Silver Spring, MD 20910-7500, USA.

出版信息

Phytomedicine. 2006 Jan;13(1-2):29-36. doi: 10.1016/j.phymed.2003.11.011. Epub 2005 Jun 28.

Abstract

Seed oil of Celastrus paniculatus Willd. (CP) has been reported to improve memory and the methanolic extract (ME) of CP was shown to exhibit free-radical-scavenging properties and anti-oxidant effects in human non-immortalized fibroblasts. In the present study, we have investigated the free-radical-scavenging capacity of CP seed oil (CPO) and two extracts, an ethanolic extract (EE) and a ME. CPO and EE showed dose-dependent, free-radical-scavenging capacity, but to a lesser degree than observed for ME. Oxidative stress involves the generation of free radicals and free radical scavenging is one of the mechanisms of neuroprotection. We therefore investigated the effects of CPO, ME, and EE for protection against hydrogen peroxide (H(2)O(2))- and glutamate-induced neurotoxicity in embryonic rat forebrain neuronal cells (FBNC). Pre-treatment of neuronal cells with CPO dose-dependently attenuated H(2)O(2)-induced neuronal death. Pre-treatment with ME and EE partially attenuated H(2)O(2)-induced toxicity, but these extracts were less effective than CPO for neuronal survival. In H(2)O(2)-treated cells, cellular superoxide dismutase (SOD) activity was unaffected, but catalase activity was decreased and levels of malondialdehyde (MDA) were increased. Pre-treatment with CPO, ME, or EE increased catalase activity and decreased MDA levels significantly. Also, CPO pre-treatment attenuated glutamate-induced neuronal death dose-dependently. The activity of cellular acetylcholinesterase (AChE) was not affected by CPO, ME, or EE, suggesting that the neuroprotection offered by CPO was independent of changes in AChE activity. Taken together, the data suggest that CPO, ME, and EE protected neuronal cells against H(2)O(2)-induced toxicity in part by virtue of their antioxidant properties, and their ability to induce antioxidant enzymes. However, CPO, which exhibited the least antioxidant properties, was the most effective in preventing neuronal cells against H(2)O(2)- and glutamate-induced toxicities. Thus, in addition to free-radical scavenging attributes, the mechanism of CP seed component (CP-C) neuroprotection must be elucidated.

摘要

据报道,南蛇藤(Celastrus paniculatus Willd.,CP)籽油可改善记忆力,且CP的甲醇提取物(ME)在人非永生化成纤维细胞中表现出自由基清除特性和抗氧化作用。在本研究中,我们研究了CP籽油(CPO)以及两种提取物,即乙醇提取物(EE)和ME的自由基清除能力。CPO和EE表现出剂量依赖性的自由基清除能力,但程度低于ME。氧化应激涉及自由基的产生,而自由基清除是神经保护的机制之一。因此,我们研究了CPO、ME和EE对胚胎大鼠前脑神经元细胞(FBNC)中过氧化氢(H₂O₂)和谷氨酸诱导的神经毒性的保护作用。用CPO对神经元细胞进行预处理可剂量依赖性地减轻H₂O₂诱导的神经元死亡。用ME和EE进行预处理可部分减轻H₂O₂诱导的毒性,但这些提取物对神经元存活的效果不如CPO。在H₂O₂处理的细胞中,细胞超氧化物歧化酶(SOD)活性未受影响,但过氧化氢酶活性降低,丙二醛(MDA)水平升高。用CPO、ME或EE进行预处理可显著提高过氧化氢酶活性并降低MDA水平。此外,CPO预处理可剂量依赖性地减轻谷氨酸诱导的神经元死亡。细胞乙酰胆碱酯酶(AChE)的活性不受CPO、ME或EE的影响,这表明CPO提供的神经保护作用与AChE活性的变化无关。综上所述,数据表明CPO、ME和EE部分凭借其抗氧化特性及其诱导抗氧化酶的能力保护神经元细胞免受H₂O₂诱导的毒性。然而,抗氧化特性最弱的CPO在预防神经元细胞免受H₂O₂和谷氨酸诱导的毒性方面最有效。因此,除了自由基清除特性外,还必须阐明CP种子成分(CP-C)的神经保护机制。

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